期刊
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
卷 25, 期 10, 页码 2376-2383出版社
AMER SOC NEPHROLOGY
DOI: 10.1681/ASN.2013080895
关键词
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资金
- interdisciplinary center of clinical research at the University of Wurzburg
- German Research Society (DFG)
- Swiss National Foundation [PP00P3-123346]
- Bundesministerium fur Bildung und Forschung [BMBF01 EO1004]
Hyponatremia, the most frequent electrolyte disorder, is caused predominantly by the syndrome of inappropriate antidiuresis (SIAD). A comprehensive characterization of SIAD subtypes, defined by type of osmotic dysregulation, is lacking, but may aid in predicting therapeutic success. Here, we analyzed serial measurements of serum osnnolality and serum sodium, plasma arginine vasopressin (AVP), and plasma copeptin concentrations from 50 patients with hyponatremia who underwent hypertonic saline infusion. A close correlation between copeptin concentrations and serum osnnolality existed in 68 healthy controls, with a mean osmotic threshold +/- SD of 282 +/- 4 nnOsM/kg H2O. Furthermore, saline-induced changes in copeptin concentrations correlated with changes in AVP concentrations in controls and patients. With use of copeptin concentration as a surrogate measure of AVP concentration, patients with SIAD could be grouped according to osmoregulatory defect: Ten percent of patients had grossly elevated copeptin concentrations independent of serum osmolality (type A); 14% had copeptin concentrations that increased linearly with rising serum osmolality but had abnormally low osmotic thresholds (type B); 44% had normal copeptin concentrations independent of osmolality (type C), and 12% had suppressed copeptin concentrations independent of osmolality (type D). A novel SIAD subtype discovered in 20% of patients was characterized by a linear decrease in copeptin concentrations with increasing serum osmolality (type E or barostat reset). In conclusion, a partial or complete loss of AVP osnnoregulation occurs in patients with SIAD. Although the mechanisms underlying osmoregulatory defects in individual patients are presumably diverse, we hypothesize that treatment responses and patient outcomes will vary according to SIAD subtype.
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